PP.28.01: INHIBITION OF NF-B BY GINSENOSIDE RB1 AMELIORATES OXIDATIVE STRESS-INDUCED SENESCENCE. (June 2015)

• Record Type: Journal Article
• Authors: Qian, X.; Song, Z.; Yu, S.; Liu, D.; Zhou, B.; Wu, L.; Wang, M.; Zhu, J.
• Is Part Of: Journal of hypertension. Volume 33(2015)Supplement 1
• Publication Date: 2015-06
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000468540.56866.f6
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: Aging is referred to the accumulation of physical and psychological changes in a person as age increases. Senescence is the process of aging. Previous study has demonstrated NF-κb p65 plays an important role in the progress of senescence and inflammation. Ginsenoside Rb1(GRb1) can reverse endothelial cell senescence. This study is performed to explore the role of activated NF-κb p65 in senescence. Design and method: Human umbilical vein endothelial cells (HUVECs) senescence was induced by hydrogen peroxide (H2O2). NF-κb p65 inhibition was achieved by RNA interfering (RNAi) technology. PAI-1, ICAM-1, p-NF-κB p65 and NF-κB p65 was evaluated by immunoblot or real-time PCR. Senescence-associated beta-galactosidase (SA-β-gal) staining was used to identify the phenotype of cellular senescence. Results: Senescence was induced by 60 μM H2O2 in the primary human umbilical vein endothelial cells. NF-κb p65 was activated by 60 μM H2O2 in a time dependent manner. Inflammatory factor ICAM-1 was expressed more in the 60 μM H2O2 group. In the culture medium, the secretory type of ICAM-1 was also increased. Both PAI-1 and ICAM-1's expression were decreased when pretreated with GRb1 compared to H2O2 only group. PAI-1 was decreased significantly when NF-κB p65 was inhibited, and ICAM-1 expression was decreased both in basal and senescent conditions. GRb1 alleviated HUVEC senescence, ICAM-1 protein and mRNA expression and the activation of NF-κB p65. Inhibition of NF-κb p65 could prevent the senescence. Conclusions: Activation of NF-κB p65 contributes to oxidative stress-induced senescence, while Rb1 is able to attenuate HUVECs senescence partially via inhibiting NF-κB p65 activation.